Normal function · from ai-gene-review (Q5VWK5, commit 79fe13b38970) · AI-generated, not KB evidence

IL23R encodes the interleukin-23 receptor, the IL-23-specific subunit of the heterodimeric IL-23 receptor complex. IL23R pairs with IL12RB1 to form the functional receptor for IL-23 (a p19/p40 heterodimeric cytokine). IL23R is a single-pass type I membrane glycoprotein containing an N-terminal Ig-like domain and two fibronectin type III domains in its extracellular region, a single transmembrane helix, and a cytoplasmic tail bearing tyrosine motifs that recruit JAK2 and STAT3. Upon IL-23 binding, the receptor activates the JAK2/TYK2-STAT3/STAT4 signaling cascade, with predominant STAT3 activation distinguishing IL-23 signaling from IL-12 signaling. IL23R is expressed on Th17 cells, gamma-delta T cells, group 3 innate lymphoid cells, NKT cells, and NK cells, where it drives type 17 immune responses critical for mucosal immunity and defense against extracellular pathogens. The R381Q variant (rs11209026) in the cytoplasmic domain is strongly protective against inflammatory bowel disease and psoriasis, consistent with the causal role of IL-23 signaling in autoimmune inflammation.

IL23R is the IL-23-specific subunit of the heterodimeric IL-23 receptor. It binds IL-23 p19 through its N-terminal Ig domain and pairs with IL12RB1 (which binds IL-12 p40) to form the signaling-competent receptor complex. IL23R constitutively associates with JAK2 and, upon IL-23 binding, recruits STAT3, activating the JAK2/TYK2-STAT3 cascade that drives Th17 gene expression programs.
In the knowledge base · computed from kb/ at build time

Disorders

Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.

DisorderRelationshipWhere the gene appears
Legg-Calve-Perthes Disease risk factor
mechanism: Necrotic-Bone DAMP Release and Chronic Hip Synovitis
Ankylosing Spondylitis untyped
Risk Factor
mechanism: IL-23/IL-17 Axis Activation
Crohn Disease untyped
Risk Factor
mechanism: IL-23/Th17 Axis Dysregulation
Psoriasis untyped
Risk Factor
mechanism: IL-23/IL-17 Axis
Ulcerative Colitis untyped
Risk Factor
mechanism: Dysregulated Immune Response
Mechanism modules · computed from kb/

Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.